Single-Cell Transcriptomic Landscape of Smoking-Related Periodontitis

Area of Science:

• Oral Biology
• Immunology
• Genomics

Background:

• Periodontitis is a common inflammatory disease affecting gums.
• Smoking is a major risk factor exacerbating periodontitis severity.
• Understanding the cellular and molecular mechanisms of smoking-related periodontitis (SPD) is crucial.

Purpose of the Study:

• To investigate the cellular composition and molecular microenvironment of SPD.
• To identify key cell types and molecular pathways involved in SPD pathogenesis.

Main Methods:

• Single-cell RNA sequencing (scRNA-seq) on periodontal tissues from healthy, periodontitis, and SPD patients.
• Immunofluorescence validation of key gene expression and cell subtypes.
• Analysis of cellular senescence, chemokine secretion, and cell-cell interactions.

Main Results:

• Gingival epithelial cells were significantly impacted by smoking, showing senescence and increased CXCL16 secretion in SPD.
• A specific subset of CXCR6+ regulatory T cells (Tregs) was identified in SPD.
• CXCR6+ Tregs may be recruited by epithelial cells via the CXCL16-CXCR6 axis and influence Th17 cell differentiation and inflammation.

Conclusions:

• Gingival epithelial cells in SPD undergo senescence and release chemokines.
• Senescent epithelial cells may recruit CXCR6+ Tregs, potentially modulating Th17 cell responses.
• These findings offer insights into the molecular basis of SPD.